Caffeine is among the most widely consumed bioactive compounds worldwide and remains a target of cardiovascular counseling despite heterogeneous evidence across mechanistic, interventional, and epidemiologic studies. At dietary doses, caffeine acts as a competitive antagonist of adenosine receptors, influencing autonomic tone, vascular resistance, and myocardial electrophysiology. Acute exposure can produce increases in blood pressure, alterations in sympathetic activity, and changes in ventricular ectopy, whereas habitual coffee consumption is associated in cohort studies with neutral or modestly favorable cardiovascular outcomes, including lower risks of cardiovascular mortality, heart failure, and stroke at moderate intake levels. Evidence from randomized and observational studies does not support a consistent proarrhythmic effect of habitual coffee consumption, and recent clinical trials challenge recommendations for caffeine restriction in conditions such as atrial fibrillation. Importantly, caffeine exposure is heterogeneous: energy drinks and concentrated caffeine products demonstrate more consistent electrophysiologic and hemodynamic effects, including QTc prolongation and sustained blood pressure elevation, suggesting a distinct risk profile compared with coffee or tea. Genetic variability in caffeine metabolism and differences in exposure patterns further modify individual responses. Overall, current evidence supports a dose-, source-, and patient-specific framework for interpreting caffeine exposure in cardiovascular medicine rather than universal restriction.
Neshat et al. (2026) studied this question.